Individuals of lower socio-economic position (SEP) develop diseases earlier and die earlier on average compared with their more advantaged counterparts. So ubiquitous is the association between SEP and health that it has been referred to as a ‘fundamental’ cause of disease. The damaging effects of low life course SEP can be seen in every major organ system of the human body which suggests that there are common biological pathways and mechanism(s) conveying increased risk for premature ageing. Recently, DNA methylation (DNAm) has emerged as a leading biomarker of ageing and evidence is growing to support its central role as a fundamental cause of ageing. Nevertheless, the recognition that ageing is affected more by environmental as opposed to genetic factors broadens our view of ageing beyond a narrow biological focus to encompass a wider range of social (e.g. socio-economic position) and ecological influences on the pace of ageing. I propose an ambitious programme of transdisciplinary research that will integrate the social and biological hallmarks of ageing using DNAm data. The primary aim is to elucidate the causal mechanisms through which SEP gets transduced at a more fundamental cellular or molecular level to precipitate earlier ageing of the socially disadvantaged. This proposal draws upon my existing expertise with longitudinal cohort studies of development and ageing and will employ cutting-edge statistical techniques, alongside ‘omics-based’ technologies, to provide new insights into the social epidemiology of the ageing process. The methodological approach will incorporate epidemiological (i.e. prospective cohort studies), naturalistic (i.e. twin studies) and experimental designs (i.e. challenging cells) to help elucidate whether DNAm serves as a biological intermediary between SEP and premature mortality.A large number of individual studies (8, 35-37) and meta-analyses (3, 4, 31) have documented socio-economic differentials in the pace of epigenetic ageing, but the paucity of longitudinal studies means the dynamics and persistence of embedding remains shrouded (7, 29). Presently, we have no resolution concerning when these differences first emerge, nor whether they widen, narrow, or remain stable over time. The epigenetic clock does not tick at a constant rate, but runs fastest in early life, settling into a more constant rate post-puberty, mirroring processes of physical growth and development. A recent study study suggests that mean DNAm changes are largest in infancy, changing by 3% per year compared with 0.1% per year in adulthood. I therefore hypothesise that early childhood represents a sensitive period for the biological embedding of SEP.